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Thromb Haemost 2001; 85(01): 165-170
DOI: 10.1055/s-0037-1612920
Review Article
Schattauer GmbH

Serum Prostaglandin D Synthase Level after Coronary Angioplasty May Predict Occurrence of Restenosis

Teruo Inoue
1   Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine Koshigaya, Suita, Japan
,
Kan Takayanagi
1   Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine Koshigaya, Suita, Japan
,
Shigenori Morooka
2   Health Service Center, University of Tokyo, Tokyo, Japan
,
Yoshio Uehara
2   Health Service Center, University of Tokyo, Tokyo, Japan
,
Hiroshi Oda
3   Central Research Institute, Maruha Corporation, Tsukuba, Japan
,
Kousuke Seiki
3   Central Research Institute, Maruha Corporation, Tsukuba, Japan
,
Hiroshi Nakajima
3   Central Research Institute, Maruha Corporation, Tsukuba, Japan
,
Yoshihiro Urade
4   Core Research for Evolutional Science and Technology, Japan, Science and Technology Corporation, c/o Department of Molecular and Behavioral Biology, Osaka Bioscience Institute, Suita, Japan
› Author Affiliations
Further Information

Publication History

Received 04 May 2000

Accepted after revision 25 July 2000

Publication Date:
08 December 2017 (online)

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Summary

Lipocalin-type prostaglandin D synthase (L-PGDS), which is responsible for the biosynthesis of PGD2, has recently been found to be present in the atherosclerotic plaque of the human coronary artery and also to be secreted in human serum. We measured the serum L-PGDS level and compared it with the expressions of the platelet membrane surface glycoprotein and neutrophil adhesion molecule in patients undergoing PTCA. The L-PGDS level significantly decreased (P < 0.01) and the platelet surface expression of CD62P (P-selectin) significantly increased (P < 0.01) immediately after PTCA in the coronary sinus blood. Both changes were inversely correlated (R = −0.72, P < 0.001). Although the L-PGDS level in the coronary sinus blood remained equivalent to the baseline level in patients who experienced restenosis, the level increased over the baseline level (P < 0.01) at 48 h after PTCA in patients without restenosis. Neutrophil surface expression of CD11b (a subunit of Mac-1) significantly increased at 24 h (P < 0.01) to 48 h (P < 0.001) after PTCA in the coronary sinus blood in patients with restenosis but the change showed less significant in patients without restenosis. The changes in the L-PGDS level and the CD11b expression at 48 h after PTCA were inversely correlated (R = −0.55, P < 0.05). An increased serum L-PGDS level at 48 h after PTCA possibly predicts the avoidance of late restenosis. It is suggested that reduction in PGD2 synthesis triggers platelet activation and that a subsequent increase in the PGD2 synthesis suppresses inflammatory reaction at the intervention site indicated by neutrophil activation and inhibits development of restenosis. Pharmacological or biological intervention that increases endogenous PGD2 synthesis should be tested as a new strategy to prevent restenosis.

Keywords

Prostaglandin D synthase - prostaglandin D2 - platelet - neutrophil - restenosis
 

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